Bronchial Reactivity to Cigarette and Cigar Smoke

The change in specific airway conductance produced by smoking a cigarette under standard conditions was measured in 91 heavy smokers. Subsequently 19 of the most reactive subjects smoked two cigarettes with different filters and another containing cigar tobacco. The results indicated that reactivity to cigarette smoke was reduced significantly by increasing the retention efficiency of the filter and that reactivity to inhaled cigar-tobacco smoke was no less than that to cigarette smoke.     

A Rat Model of Cigarette Smoke Abuse Liability

We sought to develop a rat model of cigarette smoke exposure (CSE) that created cotinine serum levels comparable to those of smokers and induced conditioned place preference (CPP) suggestive of cigarette smoke abuse liability. Rats were exposed to sidestream cigarette smoke delivered semicontinuously for 2 periods of 20 (group S20), 40 (group S40), or 60 (group S60) min daily for 12 wk. Serum cotinine concentration in blood samples was determined at 1 and 20 h after CSE. A biased (black versus white chamber) CPP paradigm was used. In the high CSE group (group S60), serum cotinine at 1 h (250 to 300 ng/mL) was comparable to average cotinine levels reported for addicted smokers (around 300 ng/mL). Cotinine levels at 20 h after CSE were higher than the smoker–nonsmoker cut-off value (greater than 14 ng/mL) in all smoking groups, with the S60 group having the highest levels. All rats preferred the black chamber to the white chamber during the preexposure CPP test. The time spent in the white chamber was increased compared with 0-wk values in group S40 at 8 wk, group S60 at 4 and 8 wk, and the control group at 4 and 8 wk but not at 12 wk; however, the shift in CPP was significantly higher at 8 wk in group S60 compared with other groups. In conclusion, interrupted 2-h daily CSE for 8 wk induced serum cotinine levels in rats comparable to those of smokers and induced CPP suggestive of cigarette smoke abuse liability.Abbreviations: CPP, conditioned place preference; CSE, cigarette smoke exposureThe devastating consequences of smoking on health have been studied extensively in numerous clinical and animal studies over time. This chronic habit leads to dependence on tobacco smoke, with nicotine, a main active ingredient of tobacco products, being recognized as the basic addictive substance.³²The known health benefits of smoking cessation motivate smokers to quit tobacco use. However, unaided efforts usually are unsuccessful, resulting in smoking relapse. The fight against nicotine addiction may be undermined by potential weight gain after smoking cessation, potentially discouraging those attempting to quit smoking and contributing to relapse. During the past few years, research has been focused on 2 main areas of interest toward this direction: understanding the underlying biologic mechanisms related to nicotine addiction to effectively design therapeutic strategies to support those who wish to quit smoking and investigating the hormonal and molecular mechanisms responsible for weight gain after smoking cessation.So far, animal models used to study the consequences of smoking cessation involved the administration of nicotine as a sole agent until addiction was achieved.²³ However, nicotine-administration models do not completely represent the toxic and addictive effects of cigarette smoke, given that smoke contains more than 4000 chemicals whose actions or coactions have not been thoroughly evaluated yet.¹ Cigarette smoke exposure (CSE) animal models have been used in studies investigating the metabolic changes conferred by smoking^10-12 but not in those after its cessation. In toxicity studies, animals are exposed to tobacco smoke for various periods, which depend on the side effect under investigation.^18,25,27 Smoke exposure timetables usually do not involve weekends for practical reasons, and addiction of animals to tobacco smoke is not assessed in current models.In our opinion, an ideal animal model of cigarette smoke abuse liability suitable for the study of smoking cessation resembles the clinical situation in terms of chronic daily inhalation of cigarette smoke sufficient to attain blood nicotine levels comparable to those of smokers and in cessation of the CSE period after achieving tobacco smoke abuse liability. In the present project, we sought to establish such a model in rats by defining the daily timetable of CSE to induce serum levels of cotinine, nicotine''s major proximate metabolite, comparable to those of smokers and by determining the minimum total CSE period required to induce abuse liability to cigarette smoke. We assessed the CSE period by using a biased conditioned place preference (CPP) paradigm.⁸     

Patterns and associations of smoking and electronic cigarette use among survivors of tobacco related and non-tobacco related cancers: A nationally representative cross-sectional analysis

BackgroundTobacco-use among cancer survivors leads to preventable morbidity, mortality, and increased healthcare costs. We sought to explore the prevalence of smoking and e-cigarette use among survivors of tobacco and non-tobacco related cancers.MethodsA cross-sectional analysis was conducted using the 2015–2018 National Health Interview Survey. Our primary outcome was the prevalence of current cigarette smoking or e-cigarette use among adults with self-reported history of tobacco related or non-tobacco related cancer. Logistic regression analysis was to assess the association of reported cancer type with cigarette smoking or e-cigarette use. Secondary outcomes included yearly trends and dual use.ResultsA total of 12,984 respondents reported a history of cancer, representing a weighted estimate of 5,060,059 individuals with a history of tobacco-related malignancy and 17,583,788 with a history of a tobacco and non-tobacco related cancer, respectively. Survivors of tobacco-related cancers had a significantly higher prevalence of current cigarette use (18.2 % vs 9.7 %, P < 0.0001), e-cigarette use (2.7 % vs 1.6 %, P < 0.0001) and similar rates of dual use. The prevalence of cigarette smoking among all survivors increased as time increased from the year of diagnosis up to 2 years post-diagnosis (P = 0.047). Odds of reporting current cigarette smoking use was higher for survivors of tobacco-related cancers, adjusted for sociodemographic factors (OR1.69, 95 % CI 1.44−1.99).ConclusionsSurvivors of tobacco-related cancers have a higher prevalence of current cigarette smoking and e-cigarette use compared to survivors of non-tobacco related cancers. There was a sequential increase in the prevalence of cigarette use during each subsequent year from the time of a new cancer diagnosis, underscoring the need for long term tobacco cessation support among newly diagnosed adults with cancer.     

A protocol for detecting and scavenging gas-phase free radicals in mainstream cigarette smoke

Cigarette smoking is associated with human cancers. It has been reported that most of the lung cancer deaths are caused by cigarette smoking (5,6,7,12). Although tobacco tars and related products in the particle phase of cigarette smoke are major causes of carcinogenic and mutagenic related diseases, cigarette smoke contains significant amounts of free radicals that are also considered as an important group of carcinogens(9,10). Free radicals attack cell constituents by damaging protein structure, lipids and DNA sequences and increase the risks of developing various types of cancers. Inhaled radicals produce adducts that contribute to many of the negative health effects of tobacco smoke in the lung(3). Studies have been conducted to reduce free radicals in cigarette smoke to decrease risks of the smoking-induced damage. It has been reported that haemoglobin and heme-containing compounds could partially scavenge nitric oxide, reactive oxidants and carcinogenic volatile nitrosocompounds of cigarette smoke(4). A 'bio-filter' consisted of haemoglobin and activated carbon was used to scavenge the free radicals and to remove up to 90% of the free radicals from cigarette smoke(14). However, due to the cost-ineffectiveness, it has not been successfully commercialized. Another study showed good scavenging efficiency of shikonin, a component of Chinese herbal medicine(8). In the present study, we report a protocol for introducing common natural antioxidant extracts into the cigarette filter for scavenging gas phase free radicals in cigarette smoke and measurement of the scavenge effect on gas phase free radicals in mainstream cigarette smoke (MCS) using spin-trapping Electron Spin Resonance (ESR) Spectroscopy(1,2,14). We showed high scavenging capacity of lycopene and grape seed extract which could point to their future application in cigarette filters. An important advantage of these prospective scavengers is that they can be obtained in large quantities from byproducts of tomato or wine industry respectively(11,13).     

What Are the Major Determinants in the Success of Smoking Cessation: Results from the Health Examinees Study

Understanding mechanisms underlying smoking-related factors should be prioritized in establishing smoking prevention and cessation policy. The aim of this study was to identify factors significantly associated with smoking initiation and/or smoking cessation as well as the most important determinants of successful smoking cessation in a developed non-Western setting. Based on multiple logistic regression models, the odds ratios (ORs) for smoking initiation and cessation were estimated among males (N = 24,490) who had participated in the Health Examinees (HEXA) study. The Cox proportional hazards regression model was used to assess the association between selected predictors of smoking cessation and the likelihood of reaching this goal. Finally, Kaplan–Meier curves were constructed to illustrate the distribution of time from age at smoking initiation to age at smoking cessation. We found that the ORs for successfully quitting smoking increased with age, married status, educational achievement, having a non-manual job, drinking cessation and disease morbidity. Those exposed to secondhand smoking showed less likelihood of quitting smoking. A continual decrease in the ORs for successfully quitting smoking was observed according to increased smoking duration, smoking dose per day and lifetime tobacco exposure (p _trend <0.001). Among the selected predictors, lifetime tobacco exposure, educational attainment, alcohol drinking status and birth cohort were the major determinants in the success of smoking cessation. Our findings suggest that lifetime tobacco exposure, educational attainment, alcohol drinking status and birth cohort can determine success in smoking cessation. Public interventions promoting a smoke-free environment are needed to reinforce discouraging the initiation of, reducing, and quitting cigarette smoking.     

Electronic Cigarettes Efficacy and Safety at 12 Months: Cohort Study

Objective

To evaluate the safety and efficacy as a tool of smoking cessation of electronic cigarettes (e-cigarettes), directly comparing users of e-cigarettes only, smokers of tobacco cigarettes only, and smokers of both.

Design

Prospective cohort study. Final results are expected in 2019, but given the urgency of data to support policies on electronic smoking, we report the results of the 12-month follow-up.

Data Sources

Direct contact and structured questionnaires by phone or via internet.

Methods

Adults (30–75 years) were included if they were smokers of ≥1 tobacco cigarette/day (tobacco smokers), users of any type of e-cigarettes, inhaling ≥50 puffs weekly (e-smokers), or smokers of both tobacco and e-cigarettes (dual smokers). Carbon monoxide levels were tested in a sample of those declaring tobacco smoking abstinence.

Main Outcome Measures

Sustained smoking abstinence from tobacco smoking at 12 months, reduction in the number of tobacco cigarettes smoked daily.

Data Synthesis

We used linear and logistic regression, with region as cluster unit.

Results

Follow-up data were available for 236 e-smokers, 491 tobacco smokers, and 232 dual smokers (overall response rate 70.8%). All e-smokers were tobacco ex-smokers. At 12 months, 61.9% of the e-smokers were still abstinent from tobacco smoking; 20.6% of the tobacco smokers and 22.0% of the dual smokers achieved tobacco abstinence. Adjusting for potential confounders, tobacco smoking abstinence or cessation remained significantly more likely among e-smokers (adjusted OR 5.19; 95% CI: 3.35–8.02), whereas adding e-cigarettes to tobacco smoking did not enhance the likelihood of quitting tobacco and did not reduce tobacco cigarette consumption. E-smokers showed a minimal but significantly higher increase in self-rated health than other smokers. Non significant differences were found in self-reported serious adverse events (eleven overall).

Conclusions

Adding e-cigarettes to tobacco smoking did not facilitate smoking cessation or reduction. If e-cigarette safety will be confirmed, however, the use of e-cigarettes alone may facilitate quitters remaining so.

Registration Number

NCT01785537.     

A Prospective Study of Tobacco Smoking and Mortality in Bangladesh

Background

Limited data are available on smoking-related mortality in low-income countries, where both chronic disease burden and prevalence of smoking are increasing.

Methods

Using data on 20, 033 individuals in the Health Effects of Arsenic Longitudinal Study (HEALS) in Bangladesh, we prospectively evaluated the association between tobacco smoking and all-cause, cancer, and cardiovascular disease mortality during ∼7.6 years of follow-up.Cox proportional hazards models were used to estimate hazard ratios (HRs) and their 95% confidence intervals (CIs) for deaths from all-cause, cancer, CVD, ischemic heart disease (IHD), and stroke, in relation to status, duration, and intensity of cigarette/bidi and hookah smoking.

Results

Among men, cigarette/bidi smoking was positively associated with all-cause (HR 1.40, 95% CI 1.06 1.86) and cancer mortality (HR 2.91, 1.24 6.80), and there was a dose-response relationship between increasing intensity of cigarette/bidi consumption and increasing mortality. An elevated risk of death from ischemic heart disease (HR 1.87, 1.08 3.24) was associated with current cigarette/bidi smoking. Among women, the corresponding HRs were 1.65 (95% CI 1.16 2.36) for all-cause mortality and 2.69 (95% CI 1.20 6.01) for ischemic heart disease mortality. Similar associations were observed for hookah smoking. There was a trend towards reduced risk for the mortality outcomes with older age at onset of cigarette/bidi smoking and increasing years since quitting cigarette/bibi smoking among men. We estimated that cigarette/bidi smoking accounted for about 25.0% of deaths in men and 7.6% in women.

Conclusions

Tobacco smoking was responsible for substantial proportion of premature deaths in the Bangladeshi population, especially among men. Stringent measures of tobacco control and cessation are needed to reduce tobacco-related deaths in Bangladesh.     

Reducing harm from tobacco smoke exposure during pregnancy

In addition to the health risks that maternal tobacco smoke exposure in pregnancy poses to women, this is a cause of substantial fetal morbidity and mortality. In pregnancy, maternal tobacco smoke exposure can arise because women either smoke or are passively exposed to environmental tobacco smoke as a consequence of other's smoking. This article discusses the scope for clinicians to help reduce both types of tobacco smoke exposure in pregnancy, with a specific focus on available and effective interventions for smoking cessation by pregnant women. Behavioral support with smoking cessation is the only intervention that has been proven to encourage smoking cessation in pregnancy and reduces smoking rates in late pregnancy by 6 to 7%. There are physiological reasons to suspect that nicotine replacement therapy (NRT) will be less or (in)effective for smoking cessation in pregnancy when compared with its use by nonpregnant smokers. However, there are also strong theoretical reasons to suspect that NRT is likely to be safer than continued smoking in pregnancy. Consequently, this article reviews evidence for the safety and effectiveness of NRT when used for smoking cessation in pregnancy and recommendations concerning the use of NRT in pregnancy are presented.     

γH2AX: A potential DNA damage response biomarker for assessing toxicological risk of tobacco products

Differentiation among American cigarettes relies primarily on the use of proprietary tobacco blends, menthol, tobacco substitutes, paper porosity, paper additives, and filter ventilation. These characteristics substantially alter per cigarette yields of tar and nicotine in standardized protocols promulgated by government agencies. However, due to compensatory alterations in smoking behavior to sustain a preferred nicotine dose (e.g., by increasing puff frequency, inhaling more deeply, smoking more cigarettes per day, or blocking filter ventilation holes), smokers actually inhale similar amounts of tar and nicotine regardless of any cigarette variable, supporting epidemiological evidence that all brands have comparable disease risk. Consequently, it would be advantageous to develop assays that realistically compare cigarette smoke (CS)-induced genotoxicity regardless of differences in cigarette construction or smoking behavior. One significant indicator of potentially carcinogenic DNA damage is double strand breaks (DSBs), which can be monitored by measuring Ser 139 phosphorylation on histone H2AX. Previously we showed that phosphorylation of H2AX (defined as γH2AX) in exposed lung cells is proportional to CS dose. Thus, we proposed that γH2AX may be a viable biomarker for evaluating genotoxic risk of cigarettes in relation to actual nicotine/tar delivery. Here we tested this hypothesis by measuring γH2AX levels in A549 human lung cells exposed to CS from a range of commercial cigarettes using various smoking regimens. Results show that γH2AX induction, a critical event of the mammalian DNA damage response, provides an assessment of CS-induced DNA damage independent of smoking topography or cigarette type. We conclude that γH2AX induction shows promise as a genotoxic bioassay offering specific advantages over the traditional assays for the evaluation of conventional and nonconventional tobacco products.     

Tobacco cigarette smoking exacerbates aortic calcification in an early stage of myocardial infarction in a female mouse model

Despite increased social awareness, marketing restraints, tobacco taxation, and available smoking cessation rehab programs, active and passive smoking remain a worldwide challenging epidemic and a key risk factor for cardiovascular diseases development. Although cardiovascular (CV) protection is more pronounced in women than in men due to estrogenic effects, tobacco cigarette smoking exposure seems to alter this protection by modulating estrogen actions via undefined mechanisms. Premenopausal cigarette smoking women are at higher risk of adverse CV effects than non-smokers. In this study, we investigated the impact of cigarette smoking on early CV injury after myocardial infarction (MI) in non-menopausal female mice. Aortic arch calcification, fibrosis, reactive oxygen species, and gene expression of inflammatory and calcification genes were exaggerated in mice exposed to cigarette smoke (CS). These findings suggest that aortic injury following MI, characterized by vascular smooth muscle cells transdifferentiation, calcification, inflammation, and collagen deposition but not cardiac dysfunction is exacerbated with CS exposure. The novel findings of this study highlight the importance of aortic injury on short and long-term prognosis in CS-exposed MI females. Linking those findings to estrogen alteration is probable and entails investigation.     

A longitudinal study of medicaid coverage for tobacco dependence treatments in Massachusetts and associated decreases in hospitalizations for cardiovascular disease

Background

Insurance coverage of tobacco cessation medications increases their use and reduces smoking prevalence in a population. However, uncertainty about the impact of this coverage on health care utilization and costs is a barrier to the broader adoption of this policy, especially by publicly funded state Medicaid insurance programs. Whether a publicly funded tobacco cessation benefit leads to decreased medical claims for tobacco-related diseases has not been studied. We examined the experience of Massachusetts, whose Medicaid program adopted comprehensive coverage of tobacco cessation medications in July 2006. Over 75,000 Medicaid subscribers used the benefit in the first 2.5 years. On the basis of earlier secondary survey work, it was estimated that smoking prevalence declined among subscribers by 10% during this period.

Methods and Findings

Using claims data, we compared the probability of hospitalization prior to use of the tobacco cessation pharmacotherapy benefit with the probability of hospitalization after benefit use among Massachusetts Medicaid beneficiaries, adjusting for demographics, comorbidities, seasonality, influenza cases, and the implementation of the statewide smoke-free air law using generalized estimating equations. Statistically significant annualized declines of 46% (95% confidence interval 2%–70%) and 49% (95% confidence interval 6%–72%) were observed in hospital admissions for acute myocardial infarction and other acute coronary heart disease diagnoses, respectively. There were no significant decreases in hospitalizations rates for respiratory diagnoses or seven other diagnostic groups evaluated.

Conclusions

Among Massachusetts Medicaid subscribers, use of a comprehensive tobacco cessation pharmacotherapy benefit was associated with a significant decrease in claims for hospitalizations for acute myocardial infarction and acute coronary heart disease, but no significant change in hospital claims for other diagnoses. For low-income smokers, removing the barriers to the use of smoking cessation pharmacotherapy has the potential to decrease short-term utilization of hospital services. Please see later in the article for the Editors'' Summary     

Phlegm and Filters

Male mass radiography volunteers aged 40 or more were questioned about their sputum production and cigarette consumption in relation to type (filter or plain) smoked. Of 10,414 volunteers, 3,045 smoked filter cigarettes and 2,393 smoked plain cigarettes. The rate of persistent daily sputum of filter smokers (31·9%) was significantly lower than that of plain cigarette smokers (37·2%). A similar pattern was maintained when age and cigarette consumption were standardized. These figures are thought to understate the less injurious nature of filter cigarettes, since more than half of the filter smokers with persistent sputum developed this while previously smoking plain cigarettes.Whatever the reasons for the less injurious nature of filter cigarettes, it seems that cigarette smokers unable to stop smoking might suffer less from chronic bronchitis if they changed to filter cigarettes.     

Genetic clues to the molecular basis of tobacco addiction and progress towards personalized therapy

The molecular processes that underlie addiction are beginning to unfold. Genetically determined variations in dopaminergic neurotransmission predispose to nicotine dependence. In addition, tobacco use is likely to be governed by the rate at which smokers metabolize nicotine. Functional polymorphisms in CYTOCHROME P450 monooxygenases that metabolize nicotine have now been defined and it should soon be possible to identify fast nicotine metabolizers by DNA analysis. Here, we review the key neurotransmitter receptors and metabolic enzymes implicated in tobacco dependence. We explore the potential benefits of classifying smokers according to the molecular aetiology of their habit. One major benefit will be in planning effective strategies for smoking cessation. Methods of typing for alleles related to smoking behavior that might be suitable for use in clinical practice in the future will also be discussed     

Intense passionate love attenuates cigarette cue-reactivity in nicotine-deprived smokers: an FMRI study

Self-expanding experiences like falling in love or engaging in novel, exciting and interesting activities activate the same brain reward mechanism (mesolimbic dopamine pathway) that reinforces drug use and abuse, including tobacco smoking. This suggests the possibility that reward from smoking is substitutable by self-expansion (through competition with the same neural system), potentially aiding cessation efforts. Using a model of self-expansion in the context of romantic love, the present fMRI experiment examined whether, among nicotine-deprived smokers, relationship self-expansion is associated with deactivation of cigarette cue-reactivity regions. Results indicated that among participants who were experiencing moderate levels of craving, cigarette cue-reactivity regions (e.g., cuneus and posterior cingulate cortex) showed significantly less activation during self-expansion conditions compared with control conditions. These results provide evidence that rewards from one domain (self-expansion) can act as a substitute for reward from another domain (nicotine) to attenuate cigarette cue reactivity.     

Respiratory effects of non-tobacco cigarettes.

Data from the Tucson epidemiological study of airways obstructive disease on smoking of non-tobacco cigarettes such as marijuana were analysed to determine the effect of such smoking on respiratory symptoms and pulmonary function. Among adults aged under 40, 14% had smoked non-tobacco cigarettes at some time and 9% were current users. The prevalence of respiratory symptoms was increased in smokers of non-tobacco cigarettes. After tobacco smoking had been controlled for men who smoked non-tobacco cigarettes showed significant decreases in expiratory flow rates at low lung volumes and in the ratio of the forced expiratory volume in one second to the vital capacity. This effect on pulmonary function in male non-tobacco cigarette smokers was greater than the effect of tobacco cigarette smoking. These data suggest that non-tobacco cigarette smoking may be an important risk factor in young adults with respiratory symptoms or evidence of airways obstruction.     

Tobacco habit: historical, cultural, neurobiological, and genetic features of people's relationship with an addictive drug

This article reviews the cultural history of man's relationship with tobacco and the steps in the discovery of tobacco addiction. Nicotine dependence (ND) or nicotine addiction (NA), among other forms of drug addiction, continues to be a significant public health problem in the world, as it is associated with major severe diseases such as cardiovascular disease and cancer. Evidence for a genetic influence on smoking behavior and ND has prompted a search for susceptibility genes. Proof has recently accumulated that single nucleotide polymorphisms (SNPs) in the genetic region encoding the nicotinic acetylcholine receptor (nAChR) subunits α5, α3, and β4 are associated with smoking and ND. In this review, we consider tobacco as the archetype of substance addiction and describe the evolution of the tobacco habit from elite users to lower socioeconomic abusers (by mass marketing and specific targeting of vulnerable groups by the tobacco industry) to exemplify detrimental behavior with major threats to public health. Finally, we discuss the reasons for the difficulty of quitting addictions/habits and highlight possible solutions.     

Why do teens smoke? American Indian and Hispanic adolescents' perspectives on functional values and addiction

Tobacco use by the young is one of the greatest public health concerns in the United States and is targeted by a number of prevention and control programs. A fuller understanding of the social and cultural values that youths attach to smoking is important in achieving focused, effective prevention strategies. Drawing on data collected through individual and focus group interviews, this article examines reasons that Hispanic and American Indian youths give to explain their smoking. The analysis presented here focuses on two interrelated sets of reasons: the functional values of tobacco use (including mood management, peer influences, and image maintenance) and addiction. This article concludes with a discussion of the implications these data may have for prevention and cessation programs aimed at youth and outlines ideas for an anthropological research agenda on youth and tobacco.     

Country profile: Australia,New South Wales. From validation to implementation: Progressing tobacco smoking cessation among people with cancer and beyond via relevant authorities

This paper delineates how a program of tobacco smoking cessation after a cancer diagnosis was achieved by engagement of multiple stakeholders, government, and non-government authorities in one jurisdiction in Australia, New South Wales. While it had become increasingly obvious that smoking cessation imparts benefits akin to other known treatment modalities, knowledge of this generalisation is without benefit unless this information is delivered in a trusted context and means to quit are made available. Against a backdrop of little enthusiasm among clinicians, the Cancer Institute NSW, charged with implementing tobacco control strategies, decided to focus its 2017 annual colloquium on the topic. While the evidence was unequivocal, better clarity was needed that this was indeed a clinical responsibility, and on the resources needed. The Clinical Oncology Society of Australia, (COSA) a non-governmental peak national body representing cancer care professionals, addressed this challenge. The society’s governing body resolved to develop a position statement indicating how smoking cessation might be integrated within hospital-based cancer care. The position statement, endorsed by nineteen other cancer and non-cancer organisations, provided reassurance to the Institute to improve record capture of hospital smoking information; upskill all clinical staff and develop an automatic “patient opt out” referral to existing resources such as the Quitline. Early pilot work shows that people newly diagnosed with cancer who smoke and who were advised at that time to quit increased from 55% in 2016 to 72% in 2019.     

Metabolic effects of cigarette smoking.

The inverse relationship between cigarette smoking and body weight, a potent obstacle to stopping smoking, may be due in part to effects of smoking on increasing whole body metabolism. Studies examining chronic and acute metabolic effects of smoking, as well as its constituent nicotine, are reviewed. Evidence suggests the absence of a chronic effect; most studies indicate that smokers and nonsmokers have similar resting metabolic rates (RMR) and that RMR declines very little after smoking cessation. Although an acute effect due to smoking is apparent, its magnitude is inconsistent across studies, possibly because of variability in smoke exposure or nicotine intake. In smokers at rest, the acute effect of smoking (and nicotine intake) appears to be significant but small (less than 10% of RMR) and transient (less than or equal to 30 min). However, the specific situations in which smokers tend to smoke may mediate the magnitude of this effect, inasmuch as smoking during casual physical activity may enhance it while smoking after eating may reduce it. Sympathoadrenal activation by nicotine appears to be primarily responsible for the metabolic effect of smoking, but possible contributions from nonnicotine constituents of tobacco smoke and behavioral effects of inhaling may also be important. Improved understanding of these metabolic effects may lead to better prediction and control of weight gain after smoking cessation, thus increasing the likelihood of maintaining abstinence.     

Developing human laboratory models of smoking lapse behavior for medication screening

Use of human laboratory analogues of smoking behavior can provide an efficient, cost-effective mechanistic evaluation of a medication signal on smoking behavior, with the result of facilitating translational work in medications development. Although a number of human laboratory models exist to investigate various aspects of smoking behavior and nicotine dependence phenomena, none have yet modeled smoking lapse behavior. The first instance of smoking during a quit attempt (i.e. smoking lapse) is highly predictive of relapse and represents an important target for medications development. Focusing on an abstinence outcome is critical for medication screening as the US Food and Drug Administration approval for cessation medications is contingent on demonstrating effects on smoking abstinence. This paper outlines a three-stage process for the development of a smoking lapse model for the purpose of medication screening. The smoking lapse paradigm models two critical features of lapse behavior: the ability to resist the first cigarette and subsequent ad libitum smoking. Within the context of the model, smokers are first exposed to known precipitants of smoking relapse (e.g. nicotine deprivation, alcohol, stress), and then presented their preferred brand of cigarettes. Their ability to resist smoking is then modeled and once smokers 'give in' and decide to smoke, they participate in a tobacco self-administration session. Ongoing and completed work developing and validating these models for the purpose of medication screening is discussed.